RNA interference-mediated silencing of S100B improves nerve function recovery and inhibits hippocampal cell apoptosis in rat models of ischemic stroke.

Ischemic stroke is the leading cause of worldwide mortality and long-term disability in adults. This study aims to explore the effects of RNA interference (RNAi)-mediated silencing of the S100B gene on nerve function recovery and morphological changes of hippocampus cells in rat models with ischemic stroke. Sixty Wistar rats were assigned into different group. S100B and Caspase 3 mRNA and protein expressions were evaluated by RT-qPCR and Western blotting. Positive rate of S100B, NeuN, and MAP2 expressions were detected by immunohistochemistry (IHC). Water content, malondialdehyde (MDA) levels, and superoxide dismutase (SOD) activity in brain tissues were measured. Enzyme-linked immunosorbent assay (ELISA) was employed to detect serum levels of TNF-α and IL-1ß. A neurological severity score (NSS) was used to test nerve function. TUNEL assay was used to determine hippocampal cell apoptosis. Downregulation of S100B showed a lower number of S100B immune positive cells, but higher NeuN and MAP2-positive cells, increased SOD level, declined MDA level, prominently faster recovery of neurological function, decreased TRCS, TCTP, TCFP, and IE levels, an obvious increase in the number of survival neurons, a decrease in the number of apoptotic cells, notably decreased TNF-α and IL-1ß contents, as well as infarct volume, an obvious decrease in positive hippocampal cell Caspase 3 expression and protein expressions of Caspase 3 and cleaved Caspase 3. This study provides data to suggest that RNAi-mediated silencing of S100B gene could improve the recovery of nerve function while inhibiting apoptosis of hippocampal cells in rats with ischemic stroke.

Increased Expression of mir-34a-5p and Clinical Association in Acute Ischemic Stroke Patients and in a Rat Model.

BACKGROUND MiRNA is widely recognized as the most important regulator in various diseases. However, there has been little research regarding miRNA expression and its involvement in ischemic stroke. MATERIAL AND METHODS In this study, we investigated the pattern of miRNA-34a-5p expression along with its clinical application in human ischemic stroke and in an in vivo rat model. We recruited 102 cerebral ischemia patients and 97 health controls for this study. Clinical data were gathered and recorded with the help of questionnaires. Blood samples were obtained from patients within 72 h after cerebral ischemia. National Institutes of Health Stroke Scale (NIHSS), Acute Stroke Treatment (TOAST), and infarct volume were used to analyze the correlation of miRNA-34a-5p expression and clinical information. In addition, blood samples and brain tissues were collected from an established middle cerebral artery occlusion (MCAO) model consisting of 20 adult male mice at 24 h after the MCAO. Expression level of miRNA-34a-5p was detected by real-time polymerase chain reactions. RESULTS Results showed overexpression of miRNA-34a-5p in acute ischemic stroke patients blood samples compared to the controls (p<0.05). Also, large and small arterial strokes types demonstrated elevated miRNA-34a-5p expression levels. Further correlation analysis revealed a negative association between miRNA-34a-5p and NIHSS scores (r=-0.692 p<0.05) and infarct volume (r=-0.719, p<0.05). Moreover, in vivo experiment results showed significant up-regulated expression of miRNA-34a-5p in middle cerebral artery occlusion compared to controls, along with a positive correlation between miRNA-34a-5p in blood and brain (r=0.742, p<0.05). CONCLUSIONS Our results suggest there is a potential regulatory role of miRNA-34a-5p in acute ischemic stroke, which could serve as a therapeutic target or biomarker in stroke prognosis.

Differentiation of hUC-MSC into dopaminergic-like cells after transduction with hepatocyte growth factor.

Parkinson's disease (PD) is a common neurodegenerative condition causing significant disability and thus negatively impacting quality of life. The recent advent of stem cell-based therapy has heralded the prospect of a potential restorative treatment option for PD. In particular, mesenchymal stem cells derived from human umbilical cord (hUC-MSCs) have great potential for developing a therapeutic agent as such. Furthermore, hepatocyte growth factor (HGF), which shows mitogenic and morphogenetic activities in a variety of cells, including MSC, and may be implicated in the pathophysiology of PD. As such, HGF may represent a new therapeutic target for the disease. In this study, we successfully isolated and facilitated the transduction of an adenoviral vector expressing HGF (Ad-HGF) into isolated hUC-MSCs. Following transduction, the hUC-MSCs can differentiate into dopaminergic neuron-like cells secreting dopamine, tyrosine hydroxylase, and dopamine transporter. Our data suggest that hUC-MSCs have the ability to differentiate into dopaminergic neurons after transduction with Ad-HGF, providing encouraging evidence to further explore this approach to the treatment of PD.

[Expression of BCL2L12 gene in de novo acute myeloid leukemia and its clinical implications].

OBJECTIVE: To explore the expression of BCL2L12 gene and its clinical significance for de novo acute myeloid leukemia (AML). METHODS: Real-time quantitative PCR (RQ-PCR) was employed to measure the expression of BCL2L12 gene in 134 patients with de novo AML. The results were correlated with clinical features of patients. RESULTS: BCL2L12 gene transcript was determined for 134 AML patients and 49 healthy controls, with the median levels measured 0.1029 (0.0119-26.4090) and 0.2677 (0.0173-1.2858), respectively. There was a significant difference in the strength of BCL2L12 gene expression between patients and normal controls (P < 0.01). Those with lower BCL2L12 expression levels had a higher FLT3-ITD mutation rate compared with those with higher levels (27% vs. 5%, P = 0.036). Relapsed or refractory AML patients had lower expression compared with newly diagnosed patients (0.0873 vs. 0.1359, P = 0.014). There was no difference in overall survival (OS) between patients with higher and lower expression levels. However, for AML patients with a normal karyotype, the OS for those with lower expression was significant shorter (P = 0.037). CONCLUSION: De novo AML patients have a lower level of BCL2L12 gene expression. AML patients with lower BCL2L12 expression have a higher FLT3-ITD mutation rate, and most of them are relapse or refractory patients. In addition, among patients with a normal karyotype, those with a lower BCL2L12 expression have a shorter OS. Therefore, expression of the BCL2L12 gene may be used as a prognostic marker for AML patients with a normal karyotype.

[Karyotypic analysis and prognosis for 41 patients with chronic myelomonocytic leukemia].

OBJECTIVE: To analyze cytogenetic features of chronic myelomonocytic leukemia (CMML) patients and explore the relationship between cytogenetic characteristics and prognosis. METHODS: Clinical and laboratory data of 41 CMML patients were analyzed. RESULTS: The majority of CMML patients were middle-aged males. According to WHO classification, 17 (41.5%) patients were diagnosed as CMML-Ⅰ and 24 (58.5%) were diagnosed as CMML-Ⅱ. 14 (34%) of CMML patients harbored abnormal karyotypes and +8 was the most common. CMML-Ⅰpatients with abnormal karyotypes were older than those with normal karyotypes. CMML-Ⅱ patients with normal karyotypes had higher lymphocyte counts than those with abnormal karyotypes. Of 29 patients who had follow-up data, 26 died, with the median survival time being 4 (1-13) months. The median survival of patients with normal and abnormal karyotypes were 4.5 and 3.8 months, respectively (P=0.408). The median survival of CMML-Ⅰ patients with abnormal karyotypes was shorter than those with normal karyotypes (3 and 17 months, P=0.015), but no significant difference was found between the median survival of the two groups of CMML-Ⅱ patients (2.9 and 5.8 months, P=0.629). CONCLUSION: +8 has been the most common abnormal karyotype in CMML patients. The abnormal karyotype can be regarded as an indicator of poor prognosis for CMML-Ⅰ patients. Regardless of their karyotypes, CMML-Ⅱ patients have even poorer prognosis.

[Characteristics and outcome of chromosomal abnormalities in Ph negative cells of chronic myelogenous leukemia patients treated with tyrosine kinase inhibitors].

OBJECTIVE: To investigate cytogenetic features and outcome of chromosomal abnormalities in Philadelphia negative cells (Ph(-)CAs) of chronic myelogenous leukemia (CML) patients treated with tyrosine kinase inhibitors. METHODS: Clinical and laboratory data of 15 CML patients in which Ph(-)CAs occurred after tyrosine kinase inhibitors therapy were collected and analyzed. RESULTS: Of 15 cases with Ph(-)CAs, 12 patients were treated with imatinib, 2 were treated with dasatinib and 1 was treated with bosutinib. + 8 was the most common abnormality in Ph(-)CAs, which accounted for 46.7% of all. Ph(-)CAs usually occurred when Ph(+)cells decreased or disappeared due to tyrosine kinase inhibitors therapy. The average time for the appearance of Ph(-)CAs was 11.1 months (1-28 months). In 7 patients, the Ph(-)CAs have disappeared in 10.9 months (3-24 months). In such patients, no myelodysplastic syndrome or acute leukemia was observed. One patient has progressed to acute monocytic leukemia with Ph(+)cells. All remaining patients have achieved bone morrow remission, among which 11 patients achieved complete cytogenic response and 4 patients even achieved complete molecular response. CONCLUSION: The majority of Ph(-)CAs developed in CML patients are transient in nature. They may develop following imatinib, dasatinib or bosutinib therapy but do not interfere with the therapeutic effects of tyrosine kinase inhibitors.

Recombinant expression of human nerve growth factor beta in rabbit bone marrow mesenchymal stem cells.

Nerve growth factor (NGF) is required for the differentiation and maintenance of sympathetic and sensory neurons. In the present study, the recombinant expression of human nerve growth factor beta (hNGF-ß) gene in rabbit bone marrow mesenchymal stem cells (rMSCs) was undertaken. Recombinant vector containing hNGF-ß was constructed and transferred into rMSCs, the expressions of the exogenous in rMSCs were determined by reverse transcriptase PCR (RT-PCR), ELISA and Western blot, whereas the biological activity of recombinant hNGF-ß was confirmed using PC12 cells and cultures of dorsal root ganglion neurons from chicken embryos. The results showed that the hNGF-ß gene expressed successfully in the rMSCs, a polypeptide with a molecular weight of 13.2 kDa was detected. The maximal expression level of recombinant hNGF-ß in rMSCs reached 126.8012 pg/10(6) cells, the mean concentration was 96.4473 pg/10(6) cells. The recombinant hNGF-ß in the rMSCs showed full biological activity when compared to commercial recombinant hNGF-ß.

[Cytogenetic analysis of 154 case of acute myeloid leukemia with t(8;21)].

OBJECTIVE: To investigate the cytogenetic features of acute myeloid leukemia (AML) with t(8;21). METHODS: The clinical characteristics of 154 cases of acute myeloid leukemia with t(8;21) in our hospital were analyzed retrospectively. According to the chromosome karyotype, all cases were divided into three groups: the group without additional chromosome abnormality, the group with single sex chromosome loss and the group with additional chromosome abnormalities other than sex chromosome loss. RESULT: In this study, according to FAB classification, there were 127 cases of M2 (82.5%), 15 of M5 (9.7%), 6 of M4 (3.9%), 4 of M1(2.6%) and 2 of M0(1.3%). Cytogenetically, 85 (55.2%) AML patients with t(8;21) had additional chromosome abnormalities. The most common abnormalities were sex chromosome loss, of which -Y was detected in 44.1% of the male karyotype and X in 27.9%. Beside that, there were 9 cases of 9q- (5.8%), 5 of +8(3.3%),3 of +4(2.0%) and 17 of other chromosome anomalies (11.4%). In the group of t(8;21) with additional chromosome abnormalities, 11 cases (35.5%) were non-M2 AML, higher than that in single t(8;21) group (17.4%)(P<0.05); however, there was no significant difference between the group of single t(8;21) and the group of t(8;21) with single sex chromosome loss(P>0.05). CONCLUSION: t(8;21) translocation is usually accompanied by additional chromosome abnormalities, particularly in M2; while t(8;21) with additional chromosome abnormalities other than sex chromosome loss is more frequently observed in non-M2 AML.

[Karyotype analysis of 283 cases of myelodysplastic syndrome].

OBJECTIVE: To explore the implication of karyotype analysis in diagnosis and prognosis of myelodysplastic syndrome (MDS). METHODS: The chromosomes were prepared with direct method, brief culture of cells and R-banding techniques, and then the karyotypic analysis was performed. RESULT: Seventy-seven out of 283 patients (27.21%) had karyotypic abnormalities, including the numeral abnormalities of chromosomes and structural alterations. The most common chromosomal aberrations were +8, -20/20q-, -Y, translocation, -7/7q-, +9, -5/5q-. The rate of abnormal karyotype in refractory anemia with erythroblasts (RAEB) and refractory anemia erythroblasts-transformation (RAEB-t) was much higher than in refractory anemia (RA). Patients with abnormal karyotype or higher IPSS scores had a higher risk of transformation into acute leukemia than patients with normal karyotype or lower IPSS scores (P<0.05). CONCLUSION: MDS is a highly heterogenous disorder and karyotype analysis is helpful for its diagnosis and prognosis estimation.

Complete mitochondrial genome sequence of the Rattus norvegicus SILN strain with central nervous system disorder.

The Rattus norvegicus SILN strain is a common used model for nervous system disorder disease study. We sequenced this R. norvegicus strain SILN mitochondrial genome for the first time (GenBank Accession No. KM114606). Its mitogenome was 16,311 bp and coding 13 protein-coding genes, 2 ribosomal RNA genes, 22 transfer RNA genes.

Protective effect of bone marrow mesenchymal stem cells on PC12 cells apoptosis mediated by TAG1.

OBJECTIVE: This study aims to explore the protection effect of bone marrow mesenchymal stem cells (BMSCs) on PC12 cells apoptosis mediated by transient axonal glycoprotein 1 (TAG1). METHODS: PC12 cells were divided into control group, Aß25-35 group and BMSCs + Aß25-35 group. The effects of BMSCs on PC12 cells treated by Aß25-35 were detected using MTT, Hoechst 33258 and Annexin V-FITC/PI staining methods. The expression levels of TAG1, ß-amyloid precursor protein (APP), AICD and p53 were determined by RT-PCR and Western blotting methods. The expression levels of Bax and Bcl-2 were determined by Western blotting method. The activity of Caspase 3 was detected by spectrophotometric method. RESULTS: MTT results showed that cell activity decreased after the treatment of 20 µM Aß25-35 for 48 h (P<0.01) while it increased in BMSCs + Aß25-35 group (P<0.01). Hoechst 33258 and Annexin V-FITC/PI staining results showed that Aß25-35 could induce the apoptosis of PC12 cells while the apoptosis of PC12 cells was inhibited in BMSCs + Aß25-35 group. RT-PCR and Western blotting methods showed that 20 µM Aß25-35 could increase the expression levels of TAG1, APP, AICD and p53 (P<0.01) while they decreased in BMSCs + Aß25-35 group (P<0.01). 20 µM Aß25-35 could increase the expression levels of Bax and decrease the expression levels of Bcl-2 (P<0.01), while the expression levels of Bax decreased and the expression levels of Bcl-2 increase in BMSCs + Aß25-35 group (P<0.01). 20 µM Aß25-35 could enhance Caspase 3 activity while it decreased in BMSCs + Aß25-35 group (P<0.01). Conclusions BMSCs with Aß25-35 could inhibit the apoptosis of PC12 cells, which maybe related with TAG1/APP/AICD signal pathway.

Effects of dexamethasone on aquaporin-4 expression in brain tissue of rat with bacterial meningitis.

Aquaporin-4 (AQP4) is the most popular water channel protein expressed in brain tissue and plays a very important role in regulating the water balance in and outside of brain parenchyma. To investigate the expression of aquaporin-4 in the rat brain tissue after dexamethasone therapy of meningitis induced by Streptococcus pneumonia, total 40 of 3-week old Sprague-Dawley rats were divided into infection group (n=30) and normal control group (n=10). The meningitis groups were infected with 1×10(7) cfu/ml of Streptococcus pneumoniae and then randomized into no treatment (untreated group, n=10), treatment with ceftriaxone (CTRX group, n=10) and treatment with dexamethasone combined ceftriaxone (CTRX+DEXA group, n=10). The normal control group was established by using saline. The rats were euthanized when they reached terminal illness or five days after infection, followed by detection of AQP4 through using immunohistochemistry and Western blot methods. Data has showed that expression of AQP4 in model group remained higher than the control and treatment group (P<0.05). AQP4 expression in CTRX+DEXA group was lower than that in CTRX group (P<0.05). There was no statistical difference between CTRX+DEXA group and the control group (P>0.05). These data suggested that Dexamethasone could down-regulate the expression of AQP4 in the brain tissue of rats with meningitis and provides evidence for the mechanism of protective effect of Dexamethasone on central neurosystem.

[Clinical and experimental study of 38 cases with trisomy 8].

OBJECTIVE: To study the role of trisomy 8 in pathogenesis and progression of hematologic disease with trisomy 8. METHODS: The clinical data on 38 cases with trisomy 8 were investigated retrospectively. Fluorescence in situ hybridization (FISH) using Spectrum Orange labeled chromosome 8 centromere specific probe was carried out to detect trisomy 8 in 10 cases. RESULTS: Thirty-two of 38(84.2%) cases with trisomy 8, and fourteen of 17(82.4%) cases with trisomy 8 as the sole chromosome aberration were myeloid disorders such as myelodysplastic syndrome (MDS), acute myelocytic leukemia (AML), chronic myelocytic leukemia (CML). The incidence of trisomy 8 was higher in myeloid disease than in lymphocytic disease (5% vs 1.3%); the incidence of trisomy 8 was higher in acute monocytic leukemia than in other AML (6.1% vs 2.4%), and the incidence of trisomy 8 in chronic myelomonocytic leukemia( CMML) was higher than that in other myelodysplastic syndrome (MDS) (25% vs 13.2%); 17 cases had trisomy 8 as the sole chromosome aberration, 21 cases had other additional chromosome aberrations. The chromosome aberration was confirmed by FISH in 10 cases with trisomy 8 as the sole chromosome aberration. Eleven cases were treated with chemotherapy, among them only 10 cases data were available. Seven cases acquired complete remission but 3 of them were M3, the other 3 cases had no response after two courses of chemotherapy. CONCLUSION: Trisomy 8 may play an important role in the pathogenesis and progression of the hematological disease, especially myeloid disease. Trisomy 8 might be related with differentiation abnormality of monocyte.

[Analysis of 32 cases of acute leukemia with abnormality of chromosome 7].

OBJECTIVE: To explore the incidence and prognostic significance of chromosome 7 anomaly in acute leukemia. METHODS: Conventional cytogenetic analysis of R-band was used to detect the abnormalities of chromosome 7 in 410 acute leukemia patients. RESULTS: Thirty-two cases (7.8%) with abnormalities of chromosome 7, of which 19 (59.4%) had -7/7q-; 3(9.4%) had t(7;11); and the rest had other abnormalities such as der(7), +7, t(2;7), t(5;7), t(7;9), t(7;8) and dic(1;7). The incidence of -7/7q- in M0, M1 and M2 was higher than that in other subtypes of acute myeloid leukemia (AML). Twenty cases had additional cytogenetic aberrations, such as t(9;22) with -7, +8, -5. In 30 cases treated with chemotherapy, 11 cases acquired complete remission (CR) and the CR rate was lower than that for all concurrent cases of acute leukemia(36.7% vs 65.8%); the CR rate of AML with -7/7q- was lower than that of AML with normal karyotype(25% vs 55.6%). There was no difference in the CR rate between acute lymphocytic leukemia(ALL) with -7/7q- and ALL with normal chromosome (57.1% vs 77.8%), but 4 cases with -7/7q- which attained complete remission for a time relapsed early. In other 11 patients with additional chromosome 7 aberration, only 4 patients acquired CR. CONCLUSION: -7/7q- was the frequent aberration in chromosome 7 anomaly, which was often detected in M0, M1 and M2. It might be associated with the pathogenesis of acute leukemia; the patients with chromosome 7 anomaly had poorer prognosis.

The potential of human umbilical cord-derived mesenchymal stem cells as a novel cellular therapy for multiple sclerosis.

Multiple sclerosis (MS) is a complex disease of neurological disability, affecting more than 300 out of every 1 million people in the world. The purpose of the study was to evaluate the therapeutic effects of human umbilical cord-derived mesenchymal stem cell (hUC-MSC) transplantation in MS patients. Twenty-three patients were enrolled in this study, and 13 of them were given hUC-MSC therapy at the same time as anti-inflammatory treatment, whereas the control patients received the anti-inflammatory treatment only. Treatment schedule included 1,000 mg/kg of methylprednisolone intravenously (IV) daily for 3 days and then 500 mg/kg for 2 days, followed by oral prednisone 1 mg/kg/day for 10 days. The dosage of prednisone was then reduced by 5 mg every 2 weeks until reaching a 5-mg/day maintenance dosage. Intravenous infusion of hUC-MSCs was applied three times in a 6-week period for each patient. The overall symptoms of the hUC-MSC-treated patients improved compared to patients in the control group. Both the EDSS scores and relapse occurrence were significantly lower than those of the control patients. Inflammatory cytokines were assessed, and the data demonstrated a shift from Th1 to Th2 immunity in hUC-MSC-treated patients. Our data demonstrated a high potential for hUC-MSC treatment of MS. This manuscript is published as part of the International Association of Neurorestoratology (IANR) special issue of Cell Transplantation.

[Efficacy and safety of the HAA regimen as induction chemotherapy in 236 de novo acute myeloid leukemia].

OBJECTIVE: To evaluate the efficacy and safety of the HAA regimen (homoharringtonine, cytarabine and aclarubicin) as induction chemotherapy in de novo acute myeloid leukemia (AML). METHODS: The efficacy and safety of 236 de novo AML patients who received the HAA regimen as induction chemotherapy were retrospectively analyzed. The complete remission (CR) rate was assayed. Kaplan-Meier method was used to estimate overall survival (OS) and relapse free survival (RFS), and the differences were compared by Log-rank test. RESULTS: The overall CR rate was 78.0%, and 65.7% of the patients attained CR in the first induction cycle. The early death rate was 4.7%. The median followup time was 41(1-161) months. The estimated 5-year OS and 5-year RFS rates were 44.9% and 45.5%, respectively. The CR rates of patients with favorable, intermediate and unfavorable cytogenetics were 92.9%,78.6%and 41.7%, respectively. The 5-year OS of favorable and intermediate group were 61.1% and 45.1%, respectively. The 5- year RFS of favorable and intermediate group were 49.0% and 45.4%, respectively. The median survival time of unfavorable group was only 5 months. The side effects associated with the HAA regimen were tolerable, in which the most common toxicities were myelosuppression and infection. CONCLUSION: The HAA regimen is associated with a higher rate of CR and longer survival time and its toxicity could be tolerated.

[Expression and clinical significance of ID1 gene in acute myeloid leukemia].

OBJECTIVE: To explore the expression and clinical significance of ID1 gene in acute myeloid leukemia (AML) patients. METHOD: Real-time quantitative PCR (RQ-PCR) was used to test the expression level of ID1 gene in 114 de novo adult AML patients, and the clinical features of these patients were analyzed. RESULTS: ID1 gene transcript levels were detectable in BM mononuclear cells from 114 patients with AML, the median expression level of all samples was 8525 (range: 57 - 11 233 238). There was a statistically significant difference on expression level of ID1 gene among the three different cytogenetic prognosis groups, and the poor prognosis group (median: 36 840, range: 336 - 11 233 238) harbored the significantly higher level of ID1 gene than the intermediate prognosis group (Median: 6630, range: 66 - 1 840 798) (P = 0.006). The expression level of ID1 gene was positively associated with older age (age ≥ 60 years vs < 60 years, P = 0.002) and higher WBC count (WBC ≥ 10×10(9)/L vs < 10×10(9)/L, P = 0.005). Young patients (age < 60 years) who were not obtained the complete remission (non-CR) after the first cycle of chemotherapy harbored the high level of ID1 gene (Median: 9537 of non-CR vs 1268 of CR, P = 0.010). CONCLUSIONS: High expression level of ID1 gene was mostly seen in AML patients with adverse cytogenetics and older age (age ≥ 60 years), and may be associated with poor prognosis of AML. ID1 gene might be a prognostic molecular marker of AML.

[Clinical analysis on 15 acute myeloid leukemia patients with 11p15 abnormalities].

OBJECTIVE: To analyze the cytogenetic and clinical features of acute myeloid leukemia (AML) with 11p15 abnormalities and explore its influence on prognosis. METHOD: The clinical and laboratory data of AML patients with 11p15 abnormalities from the First Affiliated Hospital of Zhejiang University from 1994 to 2010 were collected and their prognosis was analyzed. RESULTS: 15 (0.87%) out of 1725 de novo AML had abnormalities of 11p15, of which 6 cases involved t(7; 11), 2 had t(1; 11) and 2 had t(11; 12). And others manifested t(2; 11), t(11; 11), t(11; 14), del (11) or inv (11) respectively. The FAB type of 15 cases with 11p15 abnormalities were M2 (10 cases), M5 (3 cases), M1 (1 case) and M4 (1 case). ALL 6 cases with t(7; 11) were M2, 5 of them showed of Auer rods in myeloid blasts. 12 of 15 patients had received chemotherapy, and 7 patients obtained complete remission (CR), the median duration of CR was only 8 months (4-12 months); Of the 15 patients, 13 died, and the median overall survival (MS) was 11 months (2-19 months). CONCLUSIONS: 11p15 abnormalities is a rare recurring chromosomal aberration in AML of which the of with the most commonly seen is t(7; 11), which has its unique clinical and laboratory characteristics. AML patients with 11p15 abnormalities had a poor prognosis.

[Expression level of CDX2 gene in acute myeloid leukemia and its clinical significance].

OBJECTIVE: To explore the expression and clinical significance of Caudal-type homeobox transcription factor 2 (CDX2) gene in acute myeloid leukemia (AML) patients. METHOD: Real time quantitative PCR (RQ-PCR) was used to test the expression level of CDX2 gene in 108 de novo AML patients and the clinical features of these patients were analyzed. RESULTS: CDX2 gene transcript levels were detectable in bone marrow mononuclear cells from 108 AML patients and 7 healthy donors, the median expression level were 1179.44 (range 14.15 - 867 961.10) and 105.30 (range 22.30 - 453.11). There was a statistically significant difference in expression level of CDX2 gene between the AML patients and normal donor (P < 0.01). All 14 patients with FLT3-ITD(+) were in CDX2 gene higher expression group (P = 0.018), including 10 patients with normal karyotype. In the 83 treated AML patients (P = 0.046) and 57 higher WBC count (≥ 10×10(9)/L, P = 0.048) patients, the higher expression level of CDX2 gene was associated with lower complete remission (CR) rates. CONCLUSIONS: Higher expression level of CDX2 gene was seen mostly in AML patients with FLT3-ITD mutation and with lower CR rates. CDX2 gene might be a prognostic molecular marker in AML patients with normal karyotype.